[1]Shapouri-Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J]. Cell Physiology, 2018, 233: 6425-6440. [2]Galván-Peña S, O'Neill LA. Metabolic reprograming in macrophage polarization[J]. Front Immunol, 2014, 5: 420. doi:10.3389/fimmu.2014.00420. [3]Williams NC, O'Neill LAJ. A role for the Krebs cycle intermediate citrate in metabolic reprogramming in innate immunity and inflammation[J]. Front Immunol, 2018, 9: 141. doi:10.3389/fimmu.2018.00141. [4]Viola A, Munari F, Sánchez-Rodríguez R, et al. The metabolic signature of macrophage responses[J]. Front Immunol, 2019, 10: 1462. doi:10.3389/fimmu.2019.01462. [5]P. Kent L, Munehiko S and Tiffany H. Metabolism supports macrophage activation[J]. Front Immunol, 2017, 8: 61-67 [6]Mills E, O'Neill LA. Succinate: a metabolic signal in inflammation[J]. Trends Cell Biol, 2014, 24: 313-320. [7]Liu PS, Wang H, Li X, et al. α-ketoglutarate orchestrates macrophage activation through metabolic and epigenetic reprogramming[J].Nat Immunol, 2017, 18: 985-994. [8]Jenkins SJ, Ruckerl D, Cook PC, et al. Local macro-phage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation[J]. Science, 2011, 332: 1284-1288. [9]Luongo TS, Eller JM, Lu MJ, et al. SLC25A51 is a mammalian mitochondrial NAD+ transporter[J]. Nature, 2020, 588: 174-179. [10]Kory N, Uit de Bos J, van der Rijt S, et al. MCART1/SLC25A51 is required for mitochondrial NAD transport[J]. Sci Adv, 2020, 6: eabe5310. doi:10.1126/sciadv.abe5310 [11]Alano CC, Tran A, Tao R, et al. Differences among cell types in NAD(+) compartmentalization:a comparison of neurons, astrocytes, and cardiac myocytes[J]. Neurosci Res, 2007, 85: 3378-3385. |